Transcriptomic and proteomic analyses of rhabdomyosarcoma cells reveal differential cellular gene expression in response to enterovirus 71 infection

Leong, Wai Fook; Chow, Vincent T. K.

doi:10.1111/j.1462-5822.2005.00644.x

Cited by 81 publications

(89 citation statements)

References 89 publications

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“…Six transcriptional proteins (brain abundant membrane signal protein, c14orf166, hnRNP K isoform a, protein inhibitor of activated STAT2, presenelin binding protein, and zinc finger protein) and two translational proteins (elongation factor 1 alpha and ubiquitin A-52) were identified as modulated in expression in the infected cell, with the general trend being strongly biased (eight out of nine) toward up-regulation of these transcriptional and translational proteins (Table 1, Transcription and Translation). Interestingly, our data appear to be in direct contrast to results with some virus infections, which found that the host translational mechanism is shut down in herpes simplex virus-, poliovirus-, influenza virus-, and enterovirus 71-infected cells (28,53,54). We also observed that HSPs were modulated during infection, which may be linked to an increase in transcription and translation, since HSPs are important in protein processing (30).…”

Section: Vol 76 2008 Modulation Of the Host Cell Proteome By T Goncontrasting

confidence: 53%

Modulation of the Host Cell Proteome by the Intracellular Apicomplexan ParasiteToxoplasma gondii

et al. 2008

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To investigate how intracellular parasites manipulate their host cell environment at the molecular level, we undertook a quantitative proteomic study of cells following infection with the apicomplexan parasite Toxoplasma gondii. Using conventional two-dimensional electrophoresis, difference gel electrophoresis (DIGE), and mass spectrometry, we identified host proteins that were consistently modulated in expression following infection. We detected modification of protein expression in key metabolic pathways, including glycolysis, lipid and sterol metabolism, mitosis, apoptosis, and structural-protein expression, suggestive of global reprogramming of cell metabolism by the parasite. Many of the differentially expressed proteins had not been previously implicated in the response to the parasite, while others provide important corroborative protein evidence for previously proposed hypotheses of pathogen-cell interactions. Significantly, over one-third of all modulated proteins were mitochondrial, and this was further investigated by DIGE analysis of a mitochondrion-enriched preparation from infected cells. Comparison of our proteomic data with previous transcriptional studies suggested that a complex relationship exits between transcription and protein expression that may be partly explained by posttranslational modifications of proteins and revealed the importance of investigating protein changes when interpreting transcriptional data. To investigate this further, we used phosphatase treatment and DIGE to demonstrate changes in the phosphorylation states of several key proteins following infection. Overall, our findings indicate that the host cell proteome responds in a dramatic way to T. gondii invasion, in terms of both protein expression changes and protein modifications, and reveal a complex and intimate molecular relationship between host and parasite.The obligate intracellular protozoan Toxoplasma gondii has evolved an intimate relationship with its host that extends to the cellular and molecular levels (82, 83). The absolute requirement for invasion of an appropriate host cell in the replication of the parasite suggests that modification of host functions is central to pathogenesis. Intuitively, this subversion of the cell must be a complex process, since host cells are not inherently programmed to provide an environment conducive to pathogens. Host cells have evolved primary lines of defense as countermeasures to pathogen invasion, establishment, and replication. These include elaborate systems, such as the phagolysosomal fusion, reactive oxygen and nitrogen intermediates, the sequestration of nutrients, and even cell suicide (apoptosis), as defenses to limit pathogen growth. The implementation of these systems and the ability of successful pathogens to mitigate their effects are ultimately mediated by changes in both the levels and activities of key proteins. While some of these changes may be transcriptionally regulated and thus potentially revealed by microarray analysis, the true effectors are proteins,...

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Section: Vol 76 2008 Modulation Of the Host Cell Proteome By T Goncontrasting

confidence: 53%

Modulation of the Host Cell Proteome by the Intracellular Apicomplexan ParasiteToxoplasma gondii

et al. 2008

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“…2). Up-regulated HSPB1 has been found in cells infected with African swine fever virus (19), enterovirus 71 (20), or FHV (23). Interestingly one HSPB1 protein spot presented an increase, whereas another HSPB1 protein spot presented a decrease, demonstrating that the up-regulated HSPB1 may not be specific to IBDV infection and that different isoforms or modifications of HSPB1 may play different roles during IBDV infection.…”

Section: Ibdv Infection Hijacking Of the Host Translation Appara-mentioning

confidence: 99%

“…Unlike microfilament-and microtubule-associated cytoskeleton, the class III IF protein vimentin and a nuclear member of IF, namely chicken lamin B2, were greatly decreased. The changes in ␣-actin (upregulated ACTA2 and down-regulated alpha actin of cardiac muscle) or TUBA2 or LAMB1 have been detected in enterovirus 71-, SARS-CoV-, and influenza virus-infected cells, respectively (20,25,42). Although these proteins may not be specific to IBDV, most of the cytoskeleton alterations detected in IBDV-infected cells were caused by IBDV infection.…”

Section: Ibdv Infection Hijacking Of the Host Translation Appara-mentioning

confidence: 99%

Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Zheng

Ling

Shi

et al. 2008

Molecular & Cellular Proteomics

108

127

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“…In addition to CHRM2, the locusencoded genes CNTNAP2, HIPK2, DGKI, EPHB6, and PTN are particularly interesting in complex neurodevelopmental phenotypes including high myopia. 39,40 CHRM4 is at Chr11: 46,406,640-46,408,107 on chromosome 11p11.2. This location also contains the genes MDK, CREB3L1, and AMBRA1.…”

Section: Discussionmentioning

confidence: 99%

Muscarinic Acetylcholine Receptor 3 Is Dominant in Myopia Progression

Lin¹,

Wan

Chen

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Numerous studies have proven that the nonselective muscarinic acetylcholine receptor (mAChR) antagonist atropine prevents the axial elongation that leads to myopia. Five distinct receptor genes (CHRM1-CHRM5), each encoding a muscarinic receptor protein (M[1]-M[5]), have been cloned. Copy number variations (CNVs), which constitute a substantial portion of genetic variability and structural genetic variants, are increasingly being recognized as modulators of human diseases. In this study, CNVs of CHRMs were detected to determine the genes associated with myopia.METHODS. Participants were divided into three groups: high myopia group (myopia of 6-10 diopters [D]), severe high myopia group (myopia ‡10 D), and control group (myopia 0.5 D). The CNVs were detected, and the relative copy number was estimated using the comparative 2ÀDDCt method. Syrian hamsters with form-deprivation myopia (FDM) were used as animal models of myopia.RESULTS. The CNVs of CHRM2, CHRM3, and CHRM4 were significantly different among the groups, and the variations were most dominant in the CHRM3. The CNVs of CHRM3 showed significant differences among all 3 groups (P ¼ 0.005). A replication cohort was collected to further confirm the association of CHRM3 CNV with myopia (P ¼ 0.011). The expression of M(3) on the sclera of the FDM Syrian hamsters was upregulated and then downregulated after atropine administration.CONCLUSIONS. CHRM3 and M(3) were suggested to play important roles in the pathogenesis of myopia and in the arrested progression of myopia by atropine. (Invest Ophthalmol Vis Sci. 2012;53:6519-6525) DOI:10.1167/iovs.11-9031 C linically significant refractive errors are the most common visual disorders. Myopia affects more than half of young adults in the world. [1][2][3] In Asian countries, the prevalence of myopia has approached epidemic proportions.4 Animal studies of myopia have shown that the nonselective muscarinic acetylcholine receptor (mAChR) antagonist atropine effectively prevents the axial elongation that leads to myopia. [5][6][7] Human clinical trials have also shown the effectiveness of daily atropine administration in reducing the progression of myopia. The mAChR family proteins are a group of neurotransmitter proteins that belong to the 7-transmembrane superfamily of receptors. Five distinct receptor genes (CHRM1-CHRM5), each encoding a muscarinic receptor protein (M[1]-M[5]) with specific pharmacological properties, have been cloned. [8][9][10] Different studies have shown the diverse effects of M(1) to M(5) on myopia; moreover, M(1) to M(5) have been proposed to play various roles in the ''stop'' signal of myopic progression. [8][9][10] In vitro studies have shown that mAChR antagonists inhibited scleral proliferation and matrix synthesis. 8-10Many studies have suggested that myopia is a complex condition with multiple causes and develops as a result of interactions between multiple genes and environmental stimuli.11 This study detected CHRM1 to CHRM5 polymorphisms by using the copy number variation (CNV) metho...

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Transcriptomic and proteomic analyses of rhabdomyosarcoma cells reveal differential cellular gene expression in response to enterovirus 71 infection

Cited by 81 publications

References 89 publications

Modulation of the Host Cell Proteome by the Intracellular Apicomplexan ParasiteToxoplasma gondii

Modulation of the Host Cell Proteome by the Intracellular Apicomplexan ParasiteToxoplasma gondii

Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus

Muscarinic Acetylcholine Receptor 3 Is Dominant in Myopia Progression

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